Did poop/gut evolve with helped fuel the Cambrian explosion?

Amazing stuff! How did bowel movement and excrement develop in the first place? Still an open question, I believe.

One animal's poop is another animal's treasure!

"The driving force behind this biological big bang, they argue in a recent Trends in Ecology & Evolution review paper, just might have been feces.

While many early animals had already appeared in the fossil record during the preceding Ediacaran period, the Cambrian explosion marked the emergence of animal guts, which naturally produced a whole bunch of animal poop. Even so, fossilized turds—known as coprolites—from this time period are hard to come by, and those that are unearthed tend not to attract much attention. Many are left to gather dust in archives, ... or simply abandoned at the dig site.

For the new study, Kimmig and co-author Russell Bicknell analyzed coprolites recovered from more than 35 deposits around the globe, all dating back to before and during the Cambrian explosion. The prehistoric poo came in all shapes and sizes, from microscopic pellets to coprolites measuring several centimeters long and packed with crushed shells and other bits of undigested food. Some had dissolved upon striking the seafloor, creating something evocatively referred to as an “exploded fecal carpet.” (Maybe those marine critters should have laid off the iceberg lettuce...)

The researchers discovered that, as the Cambrian progressed, animal dung became larger, more common, and more complex, reflecting the development of more sophisticated digestive systems. As more and more of this excrement accumulated, the study authors reason, it would have carried organic matter and valuable nutrients from the rich shallows down into the deep ocean, potentially making these environments more habitable. “Together, these fossils show animals were beginning to process and then redistribute organic matter using entirely novel pipelines ,” ... Such a “fecal revolution,” they explain, may have set the stage for an eruption of new life. ..."

From the highlights and abstract:

"Highlights

The ‘Cambrian Radiation’ comprises the rapid diversification of marine organisms and ecological niches during the Ediacaran to Cambrian Periods. It is also the time during which animals with guts first appear. The appearance of guts, in turn, leads to fecal matter, fossils of which are preserved as coprolites.

Fecal matter is rarely preserved in the Cambrian. However, in a few assemblages, the diversity and development of fecal matter are observed. There was little fecal matter available at the onset of the Cambrian, while larger and more diverse fecal matter became available by the middle Cambrian.

We assess the effect that increased availability of fecal matter had on deeper water environments and how this made such environments habitable for Cambrian organisms.

Combining these observations with data on digestive tracts and biogeochemistry of nutrient cycling in the Cambrian demonstrates that fecal matter played a significant role in driving the Cambrian Radiation.

Abstract

Coprolites—fossil material extruded from an animal’s digestive system—represent a rare insight into trophic interactions in deep time. However, while the first animals appeared about 600 million years ago, the first coprolites are only observed in the earliest Cambrian.

Conversely, in modern oceans, fecal pellets are an important part of the particulate organic carbon in the water column and the global flux of organic carbon to deep water.

In this review, we analyze the impact of the advent of fecal matter on the Cambrian Radiation by examining coprolites, analyzing animal biology, and contextualizing this through the role of fecal pellets in the oceanic nutrient cycle. We illustrate the central position of coprolites in driving the Cambrian Radiation."

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On the origin of feces: how animal poo drove Earth’s greatest evolutionary event

How an ‘explosion of excrement’ changed Earth's ecosystems forever

The Cambrian fecal revolution: Fueling the Cambrian Radiation (no public access)

A curious collection of Cambrian coprolites (fossilized poop)

How specialized intestinal cells help pythons completely digest the bones of their prey

Amazing stuff!

"... When researchers peered into the intestines of Burmese pythons, they saw cells with narrow, crypt-like structures, which contained particles ... not seen previously in other vertebrates.

To find out how the cells worked ... analyzed intestinal cells from 14 year-old Burmese pythons that had fasted for three weeks before being fed one of three diets: a normal diet of whole rodents, a low-calcium diet of de-boned prey, or deboned rodents that had been injected with calcium.

When the pythons were fasting or fed a boneless meal, the crypts in their intestinal cells were narrow and empty;

snakes that ate whole rodents or boneless rodents with added calcium had crypts chock-full of large calcium, phosphorus, and iron particles.

These crypts, the researchers say, may help the snakes deal with excess calcium after eating large animals with many bones. Surprisingly, pythons that ate whole rodents did not have any bone fragments in their droppings, suggesting that they had all been completely dissolved. ..."

From the abstract:

"Burmese pythons, Python molurus bivittatus, digest the skeleton of their prey; this must result in a high amount of calcium and phosphorus passing through the intestinal lining. To determine how Burmese pythons can process this ion influx, the effects of different nutritional diets were examined in juveniles reared in captivity using three different diets: 

a normal diet with calcium and phosphorus provided from entire rodents;

a low-calcium and phosphorus diet using rodents with no bones (‘boneless prey’); and a calcium-rich diet composed of boneless rodents supplemented with calcium carbonate (CaCO3) through intraperitoneal injections inside the prey.

The effect of these diets was analysed along the intestinal mucosa using light and electron microscopy techniques ... Blood calcium and hormone levels [parathyroid hormone (PTH) and calcitonin] were also analysed from fasting pythons and snakes repeatedly fed with either a normal prey diet or a low-calcium and -phosphorus diet (boneless rats).

The results revealed the presence of specialised cells in the intestinal epithelium that are involved in the production of calcium and phosphorus particles in fed snakes. These cells have an apical crypt possessing a multi-layered particle made of calcium, phosphorus and iron-rich nucleation elements in the centre.

In fasting snakes, this cell type has empty crypts.

When snakes are fed with boneless prey, particles are not produced by this cell type, although iron elements are located within the crypts.

When calcium supplements are added to a boneless meal, large particles fill the crypts.

When snakes are fed repeatedly with a low-calcium diet, blood calcium level drops while levels of calcitonin, and particularly of those of PTH, increase.

Therefore, Burmese pythons possess a specialised intestinal cell type involved in excreting excess dissolved calcium and phosphorus that originate from the prey and are precipitated as particles that must accumulate in the faeces.

This cell type is also found in other snake species that eat vertebrates (some Boidae and a colubrid) along with a lizard, the Gila monster, Heloderma suspectum. A broader analysis among vertebrates that ingest their prey whole and dissolve the prey skeleton would allow a thorough evolutionary analysis."

ScienceAdviser

New “bone-digesting” cell type discovered in pythons

Diet-dependent production of calcium- and phosphorus-rich ‘spheroids’ along the intestine of Burmese pythons: identification of a new cell type? (no public access)

A Burmese python devouring an alligator

About the beneficial human fungal microbiome in the gut

Good news! Not to be confused with the more familiar bacterial microbiome!

"... In experiments in mice, a fungus that lives in our digestive system helped fend off non-alcoholic fatty liver disease.

Before the team could investigate how gut-dwelling fungi might be beneficial, they had to grow them—a notoriously tricky task. So they turned to FiChips, small devices that mimic the intestinal environment. That allowed them to culture 161 fungi from more than 2100 strains present in human fecal samples. And one—Fusarium foetens—popped up in gut microbiome datasets from around the world, suggesting it might be a symbiotic partner.

To test whether the fungus was actually helpful, the researchers fed mice a high-fat, choline-deficient diet, which gives the animals a liver condition similar to metabolic dysfunction-associated steatohepatitis (MASH). A single infusion of the animals’ digestive tracts with F. foetens notably reduced their symptoms, effects which largely stemmed from a single compound called FF-C1 produced by the fungus.

“The findings … point to the fungal microbiome as a rich, untapped source of compounds that may have therapeutic potential,” ..."

From the editor's summary and abstract:

"Editor’s summary

Although fungi are prevalent in the mammalian gut, remarkably little is understood about their role in host metabolic function and disease. Zhou et al. undertook a large-scale survey of fecal and environmental fungi in humans across China (see the Perspective by Hooper and Koh). They identified a filamentous fungus called Fusarium foetens that negatively associated with the human metabolic disease phenotype metabolic dysfunction–associated steatohepatitis. Experiments in mice using cultured isolates of this species revealed that it produced diverse metabolites, including a small naphthoquinone molecule that inhibited the mammalian enzyme ceramide synthase. The metabolite and the presence of the fungus reduced ceramide accumulation and alleviated fatty liver disease in mice. ...

Structured Abstract

INTRODUCTION

... Although fungi are increasingly recognized as important members of the gut community, the role of fungal symbionts in host health and diseases and the underlying molecular mechanisms are still unknown.  ...

RATIONALE

To identify the role of fungal gut symbionts, we developed a culture method based on in situ fecal environment incubation. We used this system to show that the filamentous fungi Fusarium spp. can acclimate to an anaerobic environment and establish stable colonization in mice. We discovered that this fungus was internationally ubiquitous in sequencing data of human feces. Hence, we investigated whether gut fungi play a role in host disease and particularly in metabolic dysfunction–associated steatohepatitis (MASH) progression in mouse models.

RESULTS

We designed a fungal isolation chip (FiChip)–based optimized in situ cultivation system for gut fungi (FOCUS-G), which helps obtain more unartificial and uncultured fungi. Using FOCUS-G, we systematically isolated 2137 fungal strains from fecal samples of volunteers from five different geographical areas within China.

Using oxygen adaptability tests for gut fungal isolates, we characterized Fusarium spp. as a group of intestinal filamentous fungi that can acclimate to the anaerobic conditions that prevail in the colon.

An analysis of internal transcribed spacer (ITS) data from global intestinal fungal studies confirmed that Fusarium foetens is commonly found in the gut of various human populations.

We showed that the colons of germ-free and specific pathogen–free mice could be colonized by F. foetens with a single oral gavage.

We found that F. foetens gavage improves MASH progression in mice by altering ceramide metabolism through the inhibition of CerS6, a key enzyme in the ceramide biosynthetic pathway. We validated the role of CerS6 in F. foetens–mediated amelioration of MASH in mice by intestinal-specific Cers6 deletion and overexpression.

We used chromatographic analyses to show that F. foetens produces a secondary metabolite, FF-C1, that inhibits CerS6 activity through direct, noncompetitive binding. We showed that FF-C1 improves MASH progression and disease outcome in Cers6fl/fl mice but not in Cers6ΔIE mice.

CONCLUSION

We developed a culture method based on in situ fecal environmental incubation and identified Fusarium spp. as a group of intestinal filamentous fungi that can acclimate to an anaerobic environment. F. foetens colonization reverses MASH progression in mouse models through a secondary metabolite FF-C1, which inhibits intestinal CerS6 to reduce serum levels of ceramides.

Collectively, our findings provide a deeper insight into the biology of host-commensal fungi interactions and indicate that a fungal secondary metabolite can influence clinically relevant host metabolic pathways, offering an investigative strategy for improving the therapeutic management of such diseases."

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A symbiotic filamentous gut fungus ameliorates MASH via a secondary metabolite–CerS6–ceramide axis (no public access)

Identification of gut fungi–mediated regulation of host metabolic disease.